Bengt Zöller1, Xinjun Li, Jan Sundquist, Kristina Sundquist. 1. Center for Primary Health Care Research, Lund University/Region Skåne, Floor 11, Building 28, Entrance 72, Malmö University Hospital, S-205 02 Malmö, Sweden. bengt.zoller@med.lu.se
Abstract
AIMS: This nationwide study aimed to determine whether venous thromboembolism (VTE) shares familial susceptibility with coronary heart disease (CHD). METHODS AND RESULTS: Data from the Swedish Multigeneration Register for subjects aged 0-76 years old for the period 1964-2008 were linked to the Hospital Discharge Register and Cause of Death Register. Familial risks of VTE and CHD were examined in two ways: risk of CHD in offspring whose parents had been diagnosed with VTE, and risk of VTE in offspring whose parents had been diagnosed with CHD. The analyses were repeated separately for siblings and spouses. In total, 174 768 offspring had CHD and 56 302 VTE. No association between VTE and CHD was observed among siblings. Among offspring, a lower risk of CHD was observed in subjects whose parents had suffered from VTE [standardized incidence ratio (SIR) 0.94 (95% confidence interval (CI) 0.92-0.95)], while offspring of parents with CHD had an increased risk of VTE [SIR 1.03 (95% CI 1.01-1.04)]. In spouses of VTE patients, an increased risk of CHD was observed [SIR 1.02 (95% CI 1.01-1.03)]. Conversely, risk of VTE was increased among spouses of CHD patients [SIR 1.03 (95% CI 1.02-1.03)]. Subanalyses of cases of myocardial infarction and pulmonary embolism/deep venous thrombosis showed similar results. CONCLUSION: The familial background of CHD is different from that of VTE. The present study suggests that it is unlikely that shared disease-causing mutations exist to a large extent in the population.
AIMS: This nationwide study aimed to determine whether venous thromboembolism (VTE) shares familial susceptibility with coronary heart disease (CHD). METHODS AND RESULTS: Data from the Swedish Multigeneration Register for subjects aged 0-76 years old for the period 1964-2008 were linked to the Hospital Discharge Register and Cause of Death Register. Familial risks of VTE and CHD were examined in two ways: risk of CHD in offspring whose parents had been diagnosed with VTE, and risk of VTE in offspring whose parents had been diagnosed with CHD. The analyses were repeated separately for siblings and spouses. In total, 174 768 offspring had CHD and 56 302 VTE. No association between VTE and CHD was observed among siblings. Among offspring, a lower risk of CHD was observed in subjects whose parents had suffered from VTE [standardized incidence ratio (SIR) 0.94 (95% confidence interval (CI) 0.92-0.95)], while offspring of parents with CHD had an increased risk of VTE [SIR 1.03 (95% CI 1.01-1.04)]. In spouses of VTEpatients, an increased risk of CHD was observed [SIR 1.02 (95% CI 1.01-1.03)]. Conversely, risk of VTE was increased among spouses of CHD patients [SIR 1.03 (95% CI 1.02-1.03)]. Subanalyses of cases of myocardial infarction and pulmonary embolism/deep venous thrombosis showed similar results. CONCLUSION: The familial background of CHD is different from that of VTE. The present study suggests that it is unlikely that shared disease-causing mutations exist to a large extent in the population.
Authors: Karsten Keller; Jürgen H Prochaska; Meike Coldewey; Sebastian Göbel; Volker H Schmitt; Omar Hahad; Alexander Ullmann; Markus Nagler; Heidrun Lamparter; Christine Espinola-Klein; Thomas Münzel; Philipp S Wild Journal: Life (Basel) Date: 2022-05-14